Research Papers:

A Novel Dual Signaling Axis for NSP 5a3a induced apoptosis in Head and Neck Carcinoma

Luca D'Agostino and Antonio Giordano _

PDF  |  HTML  |  How to cite

Oncotarget. 2011; 2:1055-1074. https://doi.org/10.18632/oncotarget.306

Metrics: PDF 2732 views  |   HTML 5040 views  |   ?  


Luca D’Agostino1,2 and Antonio Giordano1,2

1 Sbarro Institute for Cancer Research and Molecular Medicine & Department of Biology, College of Science and Technology Temple University, 1900 North 12th street room 431, Philadelphia PA 19122, USA

2Department of Human Pathology and Oncology, University of Siena, Siena, Italy

Received: November 21, 2011; Accepted: December 8, 2011; Published: December 14, 2011;

Keywords: NSP 5a3a, Head and Neck Carcinoma, TNFR-1 signaling pathway


Luca D’Agostino, email:


NSP 5a3a is a novel structural protein found to be over-expressed in particular cancer cell lines in-vitro such as Hela, Saos-2, and MCF-7 while low to null levels were detectable in normal body tissues except for Testis [1].  This particular isoform has been identified to interact with predominantly nuclear proteins B23 [2], known to be involved in multi-faceted cellular processes such as cell division, apoptosis, ribosome biogenesis, and rRNA processing [3], as well with hnRNP-L [4], known to be involved with RNA metabolism and rRNA processing [5-6].  A previous preliminary investigation of NSP 5a3a as a potential target in Head and Neck Carcinoma revealed a novel p73 mechanism through which NSP 5a3a induced apoptosis in Head and Neck cell lines when over-expressed in-vitro.  The mechanism seemed to indicate the involvement of an unknown high molecular weight p73 isoform (140 kDA), though was independent of p53, p14, B23, and Caspase-3 [7].  Our present investigation further identified a plausible scenario, through which the involvement of TRAF2, TRADD, and DAXX along with previously unseen lower molecular weight p73 isoforms (55 and 45 kDA) induce apoptosis in Head and Neck carcinoma.  Interestingly, this novel mechanism seems to be independent of the canonical caspases involved in the intrinsic apoptotic pathway via the mitochondria as well as those participating in the death receptor pathway thru TRAF2 and TRADD.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 306